Induced G1 cell-cycle arrest controls replication-dependent histone mRNA 3′ end processing through p21, NPAT and CDK9
Proper cell cycle-dependent expression of replication-dependent histones is essential for packaging of DNA into chromatin during replication. We previously showed that cyclin-dependent kinase-9 (CDK9) controls histone H2B monoubiquitination (H2Bub1) to direct the recruitment of specific mRNA 3′ end...
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| Veröffentlicht in: | Oncogene 2010-05, Vol.29 (19), p.2853-2863 |
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| creator | Pirngruber, J Johnsen, S A |
| description | Proper cell cycle-dependent expression of replication-dependent histones is essential for packaging of DNA into chromatin during replication. We previously showed that cyclin-dependent kinase-9 (CDK9) controls histone H2B monoubiquitination (H2Bub1) to direct the recruitment of specific mRNA 3′ end processing proteins to replication-dependent histone genes and promote proper pre-mRNA 3′ end processing. We now show that p53 decreases the expression of the histone-specific transcriptional regulator
N
uclear
P
rotein,
A
taxia-
T
elangiectasia Locus (NPAT) by inducing a G1 cell-cycle arrest, thereby affecting E2F-dependent transcription of the
NPAT
gene. Furthermore, NPAT is essential for histone mRNA 3′ end processing and recruits CDK9 to replication-dependent histone genes. Reduced NPAT expression following p53 activation or small interfering RNA knockdown decreases CDK9 recruitment and replication-dependent histone gene transcription but increases the polyadenylation of remaining histone mRNAs. Thus, we present evidence that the induction of a G1 cell-cycle arrest (for example, following p53 accumulation) alters histone mRNA 3′ end processing and uncover the first mechanism of a regulated switch in the mode of pre-mRNA 3′ end processing during a normal cellular process, which may be altered during tumorigenesis. |
| doi_str_mv | 10.1038/onc.2010.42 |
| format | Article |
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N
uclear
P
rotein,
A
taxia-
T
elangiectasia Locus (NPAT) by inducing a G1 cell-cycle arrest, thereby affecting E2F-dependent transcription of the
NPAT
gene. Furthermore, NPAT is essential for histone mRNA 3′ end processing and recruits CDK9 to replication-dependent histone genes. Reduced NPAT expression following p53 activation or small interfering RNA knockdown decreases CDK9 recruitment and replication-dependent histone gene transcription but increases the polyadenylation of remaining histone mRNAs. Thus, we present evidence that the induction of a G1 cell-cycle arrest (for example, following p53 accumulation) alters histone mRNA 3′ end processing and uncover the first mechanism of a regulated switch in the mode of pre-mRNA 3′ end processing during a normal cellular process, which may be altered during tumorigenesis.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2010.42</identifier><identifier>PMID: 20190802</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337/1645 ; 631/80/641/2187 ; 631/80/86 ; 692/420/755 ; Apoptosis ; Ataxia ; Biological and medical sciences ; Cancer ; Cell Biology ; Cell cycle ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell cycle, cell proliferation ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chromatin ; Cyclin E - deficiency ; Cyclin E - genetics ; Cyclin-dependent kinase ; Cyclin-Dependent Kinase 9 - metabolism ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Cyclin-dependent kinases ; DNA biosynthesis ; DNA Replication - drug effects ; E2F protein ; E2F4 Transcription Factor - metabolism ; Fundamental and applied biological sciences. Psychology ; G1 Phase - drug effects ; G1 Phase - genetics ; Gene expression ; Gene Expression Regulation - drug effects ; Gene Knockdown Techniques ; Genes ; Genetic aspects ; HCT116 Cells ; Histone H2B ; Histones - genetics ; Human Genetics ; Humans ; Hydroxyurea - pharmacology ; Internal Medicine ; Medicine ; Medicine & Public Health ; Messenger RNA ; Molecular and cellular biology ; Molecular genetics ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oncology ; original-article ; p53 Protein ; Physiological aspects ; Polyadenylation ; Polyadenylation - drug effects ; Protein kinases ; Proteins ; Replication ; Retinoblastoma-Like Protein p130 - metabolism ; Ribonucleic acid ; RNA ; RNA 3' End Processing - drug effects ; RNA, Messenger - genetics ; siRNA ; Transcription ; Transcription, Genetic - drug effects ; Tumor Suppressor Protein p53 - metabolism ; Tumorigenesis ; Ubiquitination</subject><ispartof>Oncogene, 2010-05, Vol.29 (19), p.2853-2863</ispartof><rights>Macmillan Publishers Limited 2010</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2010.</rights><rights>Copyright Nature Publishing Group May 13, 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-c8937d1c5f13e636394f97ce667400b91374373d921af639036f87780a58f183</citedby><cites>FETCH-LOGICAL-c509t-c8937d1c5f13e636394f97ce667400b91374373d921af639036f87780a58f183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2010.42$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2010.42$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22782735$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20190802$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pirngruber, J</creatorcontrib><creatorcontrib>Johnsen, S A</creatorcontrib><title>Induced G1 cell-cycle arrest controls replication-dependent histone mRNA 3′ end processing through p21, NPAT and CDK9</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Proper cell cycle-dependent expression of replication-dependent histones is essential for packaging of DNA into chromatin during replication. We previously showed that cyclin-dependent kinase-9 (CDK9) controls histone H2B monoubiquitination (H2Bub1) to direct the recruitment of specific mRNA 3′ end processing proteins to replication-dependent histone genes and promote proper pre-mRNA 3′ end processing. We now show that p53 decreases the expression of the histone-specific transcriptional regulator
N
uclear
P
rotein,
A
taxia-
T
elangiectasia Locus (NPAT) by inducing a G1 cell-cycle arrest, thereby affecting E2F-dependent transcription of the
NPAT
gene. Furthermore, NPAT is essential for histone mRNA 3′ end processing and recruits CDK9 to replication-dependent histone genes. Reduced NPAT expression following p53 activation or small interfering RNA knockdown decreases CDK9 recruitment and replication-dependent histone gene transcription but increases the polyadenylation of remaining histone mRNAs. Thus, we present evidence that the induction of a G1 cell-cycle arrest (for example, following p53 accumulation) alters histone mRNA 3′ end processing and uncover the first mechanism of a regulated switch in the mode of pre-mRNA 3′ end processing during a normal cellular process, which may be altered during tumorigenesis.</description><subject>631/337/1645</subject><subject>631/80/641/2187</subject><subject>631/80/86</subject><subject>692/420/755</subject><subject>Apoptosis</subject><subject>Ataxia</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell cycle, cell proliferation</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chromatin</subject><subject>Cyclin E - deficiency</subject><subject>Cyclin E - genetics</subject><subject>Cyclin-dependent kinase</subject><subject>Cyclin-Dependent Kinase 9 - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Cyclin-dependent kinases</subject><subject>DNA biosynthesis</subject><subject>DNA Replication - drug effects</subject><subject>E2F protein</subject><subject>E2F4 Transcription Factor - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>G1 Phase - drug effects</subject><subject>G1 Phase - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Knockdown Techniques</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>HCT116 Cells</subject><subject>Histone H2B</subject><subject>Histones - genetics</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hydroxyurea - pharmacology</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Messenger RNA</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oncology</subject><subject>original-article</subject><subject>p53 Protein</subject><subject>Physiological aspects</subject><subject>Polyadenylation</subject><subject>Polyadenylation - drug effects</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Replication</subject><subject>Retinoblastoma-Like Protein p130 - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA 3' End Processing - drug effects</subject><subject>RNA, Messenger - genetics</subject><subject>siRNA</subject><subject>Transcription</subject><subject>Transcription, Genetic - drug effects</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumorigenesis</subject><subject>Ubiquitination</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkk-LEzEYxoMobq2evEtQxIM7Nf9mkhxL1XVxWUV6D9lM0maZJrPJDLI3P5MfyU9ihlaLsoLkEJL3l_d5H_IA8BSjBUZUvInBLAgqJ0bugRlmvKnqWrL7YIZkjSpJKDkBj3K-RghxichDcFJwiQQiM_D1PLSjsS08w9DYrqvMreks1CnZPEATw5Bil2GyfeeNHnwMVWt7G1obBrj1eYjBwt2XyyWkP759h6UA-xSNzdmHDRy2KY6bLewJPoWXn5drqAuwevtRPgYPnO6yfXLY52D9_t169aG6-HR2vlpeVKZGcqiMkJS32NQOU9vQhkrmJDe2aThD6EpiyhnltJUEa1eqiDZOcC6QroXDgs7Bq33bMtTNWCypnc-TTx1sHLPijDW4luQ_SEoxk6jIzcHzv8jrOKZQXCgiuOA141O7F_-EGoYZYoTRI7XRnVU-uDgkbSZhtSSEYyloUxdqcQdVVmt3vnyRdb7c__Hg9f6BSTHnZJ3qk9_pdKswUlNmVMmMmjKjGCn0s8Oo49XOtr_ZXyEpwMsDoLPRnUs6GJ-PHOGCcDrJnu65XEphY9PR8126PwF97NLS</recordid><startdate>20100513</startdate><enddate>20100513</enddate><creator>Pirngruber, J</creator><creator>Johnsen, S A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20100513</creationdate><title>Induced G1 cell-cycle arrest controls replication-dependent histone mRNA 3′ end processing through p21, NPAT and CDK9</title><author>Pirngruber, J ; Johnsen, S A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-c8937d1c5f13e636394f97ce667400b91374373d921af639036f87780a58f183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>631/337/1645</topic><topic>631/80/641/2187</topic><topic>631/80/86</topic><topic>692/420/755</topic><topic>Apoptosis</topic><topic>Ataxia</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell cycle, cell proliferation</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Chromatin</topic><topic>Cyclin E - deficiency</topic><topic>Cyclin E - genetics</topic><topic>Cyclin-dependent kinase</topic><topic>Cyclin-Dependent Kinase 9 - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Cyclin-dependent kinases</topic><topic>DNA biosynthesis</topic><topic>DNA Replication - drug effects</topic><topic>E2F protein</topic><topic>E2F4 Transcription Factor - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>G1 Phase - drug effects</topic><topic>G1 Phase - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Knockdown Techniques</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>HCT116 Cells</topic><topic>Histone H2B</topic><topic>Histones - genetics</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Hydroxyurea - pharmacology</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Messenger RNA</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Oncology</topic><topic>original-article</topic><topic>p53 Protein</topic><topic>Physiological aspects</topic><topic>Polyadenylation</topic><topic>Polyadenylation - drug effects</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Replication</topic><topic>Retinoblastoma-Like Protein p130 - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA 3' End Processing - drug effects</topic><topic>RNA, Messenger - genetics</topic><topic>siRNA</topic><topic>Transcription</topic><topic>Transcription, Genetic - drug effects</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumorigenesis</topic><topic>Ubiquitination</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pirngruber, J</creatorcontrib><creatorcontrib>Johnsen, S A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pirngruber, J</au><au>Johnsen, S A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induced G1 cell-cycle arrest controls replication-dependent histone mRNA 3′ end processing through p21, NPAT and CDK9</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2010-05-13</date><risdate>2010</risdate><volume>29</volume><issue>19</issue><spage>2853</spage><epage>2863</epage><pages>2853-2863</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Proper cell cycle-dependent expression of replication-dependent histones is essential for packaging of DNA into chromatin during replication. We previously showed that cyclin-dependent kinase-9 (CDK9) controls histone H2B monoubiquitination (H2Bub1) to direct the recruitment of specific mRNA 3′ end processing proteins to replication-dependent histone genes and promote proper pre-mRNA 3′ end processing. We now show that p53 decreases the expression of the histone-specific transcriptional regulator
N
uclear
P
rotein,
A
taxia-
T
elangiectasia Locus (NPAT) by inducing a G1 cell-cycle arrest, thereby affecting E2F-dependent transcription of the
NPAT
gene. Furthermore, NPAT is essential for histone mRNA 3′ end processing and recruits CDK9 to replication-dependent histone genes. Reduced NPAT expression following p53 activation or small interfering RNA knockdown decreases CDK9 recruitment and replication-dependent histone gene transcription but increases the polyadenylation of remaining histone mRNAs. Thus, we present evidence that the induction of a G1 cell-cycle arrest (for example, following p53 accumulation) alters histone mRNA 3′ end processing and uncover the first mechanism of a regulated switch in the mode of pre-mRNA 3′ end processing during a normal cellular process, which may be altered during tumorigenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20190802</pmid><doi>10.1038/onc.2010.42</doi><tpages>11</tpages></addata></record> |
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| subjects | 631/337/1645 631/80/641/2187 631/80/86 692/420/755 Apoptosis Ataxia Biological and medical sciences Cancer Cell Biology Cell cycle Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell cycle, cell proliferation Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromatin Cyclin E - deficiency Cyclin E - genetics Cyclin-dependent kinase Cyclin-Dependent Kinase 9 - metabolism Cyclin-Dependent Kinase Inhibitor p21 - metabolism Cyclin-dependent kinases DNA biosynthesis DNA Replication - drug effects E2F protein E2F4 Transcription Factor - metabolism Fundamental and applied biological sciences. Psychology G1 Phase - drug effects G1 Phase - genetics Gene expression Gene Expression Regulation - drug effects Gene Knockdown Techniques Genes Genetic aspects HCT116 Cells Histone H2B Histones - genetics Human Genetics Humans Hydroxyurea - pharmacology Internal Medicine Medicine Medicine & Public Health Messenger RNA Molecular and cellular biology Molecular genetics Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncology original-article p53 Protein Physiological aspects Polyadenylation Polyadenylation - drug effects Protein kinases Proteins Replication Retinoblastoma-Like Protein p130 - metabolism Ribonucleic acid RNA RNA 3' End Processing - drug effects RNA, Messenger - genetics siRNA Transcription Transcription, Genetic - drug effects Tumor Suppressor Protein p53 - metabolism Tumorigenesis Ubiquitination |
| title | Induced G1 cell-cycle arrest controls replication-dependent histone mRNA 3′ end processing through p21, NPAT and CDK9 |
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